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Original Research Article | OPEN ACCESS

Imidazole-thiazolidinone inhibits oesophageal cancer cell proliferation via induction of apoptosis and cell cycle arrest at S phase

Qian Wang, Yuan Yuan, Mi Jiang, Lihua Huang1, Jie Huang, Hongyuan Shen

Breast Tumor Centre, The First Hospital of Jilin University, Jilin, Changchun 130021, China;

For correspondence:-  Hongyuan Shen   Email: JeromeMcguireblc@yahoo.com   Tel:+8643181875382

Accepted: 11 December 2019        Published: 31 January 2020

Citation: Wang Q, Yuan Y, Jiang M, Huang L, Huang J, Shen H. Imidazole-thiazolidinone inhibits oesophageal cancer cell proliferation via induction of apoptosis and cell cycle arrest at S phase. Trop J Pharm Res 2020; 19(1):51-56 doi: 10.4314/tjpr.v19i1.8

© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of imidazole-thiazolidinone on oesophageal cancer (OC) cell proliferation, and the mechanism of action involved.
Methods: Human OC cells (HCE-6 and KYSE-1170) were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10 % fetal bovine serum (FBS) and 1 % penicillin/streptomycin solution at 37 I0;C for 24 h in a humidified atmosphere of 5 % CO2 and 95 % air.   After attaining 60 - 70 % confluency, the cells were treated with serum-free medium and graded concentrations of imidazole-thiazolidinone (up to 160 µM) for 24 h. Normal cell culture without imidazole-thiazolidinone served as control. Cells in logarithmic growth phase were selected and used in this study. Cell proliferation and apoptosis were assessed using 3 (4,5 dimethyl thiazol 2 yl) 2,5 diphenyl 2H tetrazolium bromide (MTT), and flow cytometric assays, respectively. The levels of expression of apoptosis-related proteins were determined using Western blotting.    
Results: Treatment of HCE-6 and KYSE-1170 cells with imidazole-thiazolidinone for 48 h led to significant and dose-dependent reduction in their proliferation, as well as significant and dose-dependent increase in the number of apoptotic cells (p < 0.05). Light microscopy revealed significant reduction in HCE-6 cell count, detached cells, reduced cell size and irregular cytoplasmic vacuoles. Imidazole-thiazolidinone treatment significantly and dose-dependently decreased HCE-6 and KYSE-1170 cell migration, and arrested HCE-6 cell cycle at S phase (p < 0.05). In HCE-6 cells, imidazole-thiazolidinone treatment significantly and dose-dependently upregulated the expressions of cleaved caspase-3/8/9 and bax, but down-regulated bcl-2 expression significantly and dose-dependently (p < 0.05). However, metalloproteinases 2 and 9 (MMP-2 and MMP-9) expressions in HCE-6 and KYSE-1170 cells were significantly and dose-dependently down-regulated by imidazole-thiazolidinone treatment (p < 0.05).   
Conclusion: The results obtained in this study suggest that imidazole-thiazolidinone suppresses OC cell proliferation via induction of apoptosis and arrest of cell cycle at S phase.

Keywords: Imidazole-thiazolidinone, Oesophageal cancer, Metastasis, Cell cycle arrest, Apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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